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Archive > Volume 32 Issue 9 > 2025,32(9):941-947. DOI:10.3872/j.issn.1007-385X.2025.09.007 Prev Next
Basic Research
Effects of formononetin on malignant biological behaviors and angiogenesis of gallbladder cancer cells via regulating the JAK/STAT signaling pathway
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Abstract:
[Abstract] Objective: To investigate the effects of formononetin on the malignant biological behavior and angiogenesis of gallbladder cancer GBC-SD cells through regulation of the JAK2/STAT3 signaling pathway. Methods: GBC-SD cells were cultured routinely, and their xenograft nude mouse models were constructed. The cells and mice were divided into control group, formononetin group, colivelin (JAK2/STAT3 activator) group, and formononetin + colivelin group. Cell proliferation, migration and invasion, and apoptosis were assessed using MTT, Transwell, and flow cytometry assays, respectively. ELISA was applied to measure the secretion levels of vascular endothelial growth factor (VEGF) in cells of each group. Vasculogenic mimicry (VM) formation assay was used to detect the tube formation ability of each group of cells. In vivo, the effects of formononetin on xenograft tumor growth were examined, and CD31 and VEGF expression in xenograft tissues were detected by immunohistochemistry. Western blotting was applied to analyze JAK2/ STAT3 phosphorylation levels in both cells and tumor tissues. Results: Formononetin significantly inhibited the proliferation, migration, and invasion of GBC-SD cells and promoted apoptosis (all P < 0.05). It also suppressed VEGF secretion and VM formation in GBC-SD cells (all P < 0.05), inhibited the growth and vascular formation of GBC-SD xenograft tumors (all P < 0.05), reduced VEGF expression in transplanted tumor tissues, and decreased phosphorylation of the JAK2/STAT3 pathway in both GBC-SD cells and their xenograft tissues. These effects of formononetin were partially reversed by colivelin (all P < 0.05). Conclusion: Formononetin inhibits GBC-SD cell proliferation, migration, invasion, and angiogenesis, and promotes apoptosis by suppressing the JAK2/STAT3 signaling pathway. The JAK2/STAT3 signaling pathway may serve as a potential therapeutic target for gallbladder cancer.
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